title: Genetic analysis of complement component 9 (C9) polymorphisms with clearance of hepatitis B virus infection.
abstract: BACKGROUND
  The complement component 9 (C9), a major cytolytic protein in the complement system, plays an important role in the immunological process. However, associations between genetic variations of the complement factor and chronic hepatitis B virus infection still need to be investigated.
  
  
  OBJECTIVE
  We hypothesized that genetic variations in the complement component 9 gene can influence the clearance of chronic hepatitis B virus infection, hepatocellular carcinoma occurrence, and onset age of hepatocellular carcinoma. To investigate the relationship between complement component 9 variations and these disease phenotypes, we performed a case-control association analysis in a Korean population.
  
  
  METHODS
  Genetic variations were identified through direct DNA sequencing and genotyped using TaqMan assay (n = 1,103). In order to investigate the relationship of complement component 9 with chronic hepatitis B virus clearance and hepatocellular carcinoma occurrence, differences in SNP and haplotype frequency distributions were analyzed using logistic and multiple regression analyses with adjusted age and gender as covariates.
  
  
  RESULTS
  Although +23189C>T polymorphism in exon 4 and C9_ht2 [T-G-C-A-C] were significantly associated with clearance of chronic hepatitis B virus infection and hepatocellular carcinoma occurrence, the association signals were not retained after multiple testing corrections.
  
  
  CONCLUSIONS
  We conclude that variations in the complement component 9 gene are unlikely to influence clearance of chronic hepatitis B virus infection and hepatocellular carcinoma occurrence. Although this preliminary result provides meaningful information, further functional investigations in other genetic factors for pathway analyses are required.
authors.affiliation: Laboratory of Genomic Diversity, Department of Life Science, Sogang University, Shinsu-dong, Mapo-gu, Seoul 121-742, Republic of Korea.
authors.forename: Joon Seol
authors.initials: JS
authors.lastname: Bae
authors.forename: Charisse Flerida A
authors.initials: CF
authors.lastname: Pasaje
authors.forename: Byung Lae
authors.initials: BL
authors.lastname: Park
authors.forename: Hyun Sub
authors.initials: HS
authors.lastname: Cheong
authors.forename: Jeong-Hyun
authors.initials: JH
authors.lastname: Kim
authors.forename: Tae Joon
authors.initials: TJ
authors.lastname: Park
authors.forename: Jason Yongha
authors.initials: JY
authors.lastname: Kim
authors.forename: Jin Sol
authors.initials: JS
authors.lastname: Lee
authors.forename: In Song
authors.initials: IS
authors.lastname: Koh
authors.forename: Hyo-Suk
authors.initials: HS
authors.lastname: Lee
authors.forename: Yoon Jun
authors.initials: YJ
authors.lastname: Kim
authors.forename: Hyoung Doo
authors.initials: HD
authors.lastname: Shin
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D003186:Complement C9 / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006509:Hepatitis B / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic
chemical_list: D003186:Complement C9